Although ERα activation modulates expression of multiple miRNAs, the reverse action of the miRNA-mediated regulation of ERα expression and subsequent downstream oncogenic signaling pathways lead to acquired resistance to standard first-line endocrine therapies [138,139] Upregulation of Let-7 and miR-29a in ERα− breast cancer cells collectively target and repress Dicer1, triggering a loss of differentiation and enhanced aggressiveness akin to the TNBC subtype [138,140]. The gene discussed is ESR1; the disease is breast cancer.